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IL-6 gene and protein expression are rapidly and transiently upregulated in the choroid in response to myopic defocus, as a result of prior form deprivation or treatment with +15 D lenses in a nitric oxide-dependent manner.

Axon degeneration occurs via an ordered sequence of events downstream of SARM1 that proceeds from ATP loss, to defects in mitochondrial movement and depolarization, followed by calcium influx, phosphatidylserine externalization, loss of membrane permeability, and ending with catastrophic axonal self-destruction.

Loss of the decoy SNARE Tomosyn enhances synaptic vesicle docking and neurotransmitter release and regulates release and plasticity differences between tonic and phasic motoneurons in Drosophila.

Analysis of molecular signatures of lifespan variation across wild yeast isolates revealed how Nature employs environment to modify genotype, gene expression, and metabolome to arrive at different lifespan, while preserving fitness in various ecological niches.

Condensation of cytosolic protein YBX1 into processing bodies reveals mechanisms for efficient and selective sorting of proteins and their cognate microRNAs into exosomes.

Analysis of insulin secretion patterns in pancreatic islets shows that microtubules control β-cell heterogeneity by regulating initiation and timing of secretion hot spot activity in parallel with Ca²⁺ signaling.

The gut microbiota of East Asians is distinct, dissociated from body mass, and self-sustains compared to White subjects from the same region, and therein may underpin a key health disparity.

Redaction, intended to obscure personal and institutional identity, reduced the gap between Black vs. White applicants in simulated review of real NIH scientific grant applications, thus providing qualified support for double-blinded models of peer review.

Dendritic patch-clamp recordings combined with two-photon imaging and glutamate uncaging reveal two types of regenerative calcium spikes in the dendrites of CA3 pyramidal neurons from rat hippocampus.

The pathogenic success of Mycobacterium tuberculosis relies in part on its ability to blunt a component of the TLR2-dependent immune response.